ABSTRACT Around the world, 93% of children under age 15 breathe toxic air every day that puts their health and development at risk. Of 7 million deaths per year attributable to air pollution, over 60% are due to exposure to household air pollution (HAP) from burning biomass fuels or kerosene for household energy needs. Such fuels burn inefficiently, producing toxic pollutants like fine particulate matter (PM2.5) and black carbon (BC). Mothers and children suffer the highest exposures, resulting in respiratory, cardiovascular, and neurologic injury. Risks to children begin in-utero. Pregnant women inhale polluted air, with ill effects on their developing fetuses and newborns, including growth restriction, preterm birth, and low birth weight. Mounting evidence suggests that HAP can impair infant and child neurocognitive development. Particulate matter deposits in brain tissue have been demonstrated; also, HAP is a medium of exposure to heavy metals. High exposures likely induce oxidative stress and systemic inflammation. There is evidence of mediating factors: maternal stress level, mother/child nutritional status, and home environment. We will explore the impact of HAP exposures on child neurocognitive development, assessing the influence of known mediating factors. Our research capitalizes on a unique opportunity flowing from a recent randomized controlled trial (RCT) in Nigeria. We randomized 324 pregnant women into groups based on fuel use: clean versus polluting. Polluting-fuel users showed: 1) increased preterm delivery, miscarriage, and reduced gestational age at delivery, 2) biomarkers of placental oxygen deprivation, 3) excessive placental vascularization, and 4) increased systemic inflammation. We further found that polluting-fuel users reported more psychosocial stress and less energy during pregnancy. We have continued to follow the RCT children (DISCOVERY COHORT), monitoring their HAP exposures. We propose now to test the hypothesis that high pre- and postnatal HAP exposure negatively impacts neurocognitive development. We will assess development in our DISCOVERY COHORT and an added VALIDATION COHORT of newborns from a new group of pregnant (3rd trimester) women. We will monitor personal HAP exposures of mothers and children, assessing biomarkers of inflammation and oxidative stress and blood levels of micronutrients and heavy metals. We aim to assess neurocognitive development from infancy to age 8 years as associated with: (1) prenatal and early childhood HAP exposures; (2) maternal psychosocial stress level, maternal and child nutritional status, and child's home environment. Impact: Results will illuminate how HAP exposures and maternal stress affect child neurocognitive development, informing policies to reduce HAP through programs that promote use of clean-fuel cookstoves. We will develop language/culturally-adapted assessments of child neurocognition?much needed in sub-Saharan Africa?and establish pilot performance norms. This will build capacity for more research of this kind in Nigeria in the future.